The outcome of hepatic B virus (HBV) infection is the result of complex interactions between replicating HBV and the innate/adaptive immune system. As an important lectin complement pathway activator, human ficolin-2 is secreted from liver cells and contributes to the clearance of viral infections and lysis of enveloped virions, which has been implicated as an anti-infection innate immune molecule. In this issue, a research group lead by Drs. Xiao- Lian Zhang and Fengling Luo, investigated the serum and liver tissue ficolin-2 levels, in a cohort of individuals with chronic HBV infections, hepatocellular carcinoma (HCC) and liver cirrhosis. And their findings suggest that serum and intrahepatic ficolin-2 levels may be considered as one of the indicators for the response of chronic HBV infection, HCC and cirrhosis. The cover image shows the decreased ficolin-2 expression in HCC cells compared to adjacent normal hepatic cells from HCC patients. See page 249–260 for details.
Japanese encephalitis is a mosquito borne disease and is the leading cause of viral encephalitis in the Asia-Pacific area. The causative agent, Japanese encephalitis virus (JEV) can be phylogenetically classified into five genotypes based on nucleotide sequence. In recent years, genotype I (GI) has displaced genotype III (GIII) as the dominant lineage, but the mechanisms behind this displacement event requires elucidation. In an earlier study, we compared host variation over time between the two genotypes and observed that GI appears to have evolved to achieve more efficient infection in hosts in the replication cycle, with the tradeoff of reduced infectivity in secondary hosts such as humans. To further investigate this phenomenon, we collected JEV surveillance data on human cases and, together with sequence data, and generated genotype/case profiles from seven Asia-Pacific countries and regions to characterize the GI/GIII displacement event. We found that, when comprehensive and consistent vaccination and surveillance data was available, and the GIII to GI shift occurred within a well-defined time period, there was a statistically significant drop in JEV human cases. Our findings provide further support for the argument that GI is less effective in infecting humans, who represent a dead end host. However, experimental investigation is necessary to confirm this hypothesis. The study highlights the value of alternative approaches to investigation of epidemics, as well as the importance of effective data collection for disease surveillance and control.
In this report, we presented the construction of an infectious full-length clone and a recombined EV71 cDNA clone, from which the RNA transcripts could result in CPE in transfected cells. Furthermore, we also found that the 5′UTR of EV71 could influence the replication of EV71, potentially acting as a determinant of the virulence of EV71. Our results provide important insights into the pathogenic mechanisms of EV71-related diseases.
The main aim of this study is to determine whether the recent fox rabies outbreaks represent an occasional fluctuation in the borders of rabies virus habitat or it isa step toward widespread dissemination of fox rabies in Asia. According to data presented at the conference “Towards the elimination of rabies in Eurasia” (Fu, 2008; Gruzdev, 2008; Seimenis, 2008) at the beginning of the twenty-first century, fox rabies was largely unknown in the Far East while being endemic in Eastern Europe. Further, the incidence of fox rabies decreased in Central and Western Europe, while a progression occurred in the Middle East and Central Asia. Therefore, further researches are necessary on the intermediate zone between the two different rabies virus lineages in Central Asia.